Neuroradiology(1991) 33:269~71
Neuro--
radiology 0 Springer-Verlag1991
CT and MR imaging of CNS lymphomatoid granulomatosis R. Kerslake 1 D. Rowe 2, and B. S. Worthington 1 Department of Radiology,Queen's MedicalCentre, Nottingham,UK 2 Department of Neurology,RoyalHallamshireHospital,Sheffield,UK Received: 24 July 1990
Summary. The clinical CT and MR imaging features of a pathologically confirmed case of lymphomatoid granulomatosis are presented. The disease was clinically confined to the central nervous system and the diagnosis was only made after brain biopsy had been performed. MR imaging revealed extensive non-confluent regions of white matter abnormality. Although uncommon, lymphomatoid granulomatosis should be included in the differential diagnosis of causes of periventricular and deep white matter lesions, even in the absence of pulmonary lesions. Specific therapy may produce clinical regression of disease. Key words: Brain, disease - Lymphomatoid granulomatosis - Brain, computed tomography- Brain, MR imaging Lymphomatoid granulomatosis (LG) is an "angiocentric and angiodestructive lymphorecticular proliferative and granulomatous disease" which predominantly involves the lungs [1]. A small number of cases with clinically isolated central nervous system (CNS) involvement at presentation have been reported [2, 3]. In the absence of systemic disease, the diagnosis may be considerably delayed or only made at autopsy [3-5]. We report a case of lymphomatoid granulomatosis clinically confined to the CNS in which the diagnosis was established by brain biopsy during the lifetime of the patient. Both CT and MR imaging demonstrated unusually extensive abnormalities though a specific diagnosis could not be made based on the imaging findings. Awareness of the spectrum of appearances on CT and MRI may permit the correct diagnosis to be suggested at an earlier stage, allowing institution of appropriate therapy.
Case report A 44-year-old female presented with a four week history of personality change, depression and irritability. She subsequently was observed to become increasingly weak, uncoordinated, obtunded and to develop an asymmetric
tetraparesis with a degree of ataxia. She was transferred from psychiatric to general medical and subsequently to neurological care. The only past history of note was a grade II-III CIN cervical lesion, treated by cone biopsy, with no evidence of recurrence at regular follow-up. At the time of admission to the neurological unit, she was afebrile, uncooperative and mute. There was no evidence of meningeal irritation or raised intracranial pressure. Neurological examination revealed an asymmetric spastic tetraparesis principally involving the left leg. An EEG showed widespread mixed irregular and rhythmic slow activity but without focal features. Cranial CT scanning (not shown) revealed multiple poorly defined regions of low attenuation in the basal ganglia, thalami and deep white matter of both cerebral hemispheres. These were without mass effect and showed no enhancement after the intravenous injection of iodinated contrast material. Examination of the CSF showed an elevated protein concentration (0.8 g/l) but no other abnormality. Chest radiography was entirely normal. MR imaging was carried out on a 0.15T resistive system. Multiple lesions were present in both cerebral hemispheres, the left cerebellar hemisphere and in the brain stem. The lesions were large, non-confluent, well demarcated and without mass effect. On T2-weighted images (Fig. i a) they were of high signal intensity whilst on inversion recovery images (Fig. 1 b), there was central hypointensity with a peripheral zone of intermediate signal intensity. Some of the larger lesions extended to involve the sub-cortical white matter. The corpus callosum was not involved. She deteriorated relentlessly and there was no response to a 5 day course of ACTH. Brain biopsy was then performed. The pathological findings were of white matter showing a heavy infiltrate of inflammatory cells which were principally large lymphocytes, plasma cells, histiocytes and some larger atypical cells with prominent nucleoli. The inflammatory infiltrate was markedly angiocentric and the walls of small vessels were infiltrated by a mixture of these chronic inflammatory cells. Patchy necrosis of the surrounding white matter was noted and
270
Fig. 1. Axial T2-weighted (SE 2000/80) images (a) and coronal inversion recovery (IR 1660/400/40)images (b) of biopsy-provenlymphomatoid granulomatosis. There are extensive, asymmetrical lesions mainly affecting the deep white matter of the right temporal lobe and external capsule, the left pons and cerebellar hemisphere and both posterior frontal/parietal lobes.Further lesions are present in the left parieto-occipital cortex these regions contained foamy histiocytes and some reactive histiocytes. A pathological diagnosis of lymphomatoid granulomatosis was made. Treatment with pulsed methylprednisolone and cyclophosphamide was commenced and the progressive improvement in her physical state was such that discharge to the community was possible 4 months after first presentation. She relapsed clinically 3 months later. There was clinical improvement following a further course of methylprednisolone and cyclophosphamide.
Discussion
In the original description of lymphomatoid granulomatosis in 1972, Liebow described a predominantly pulmonary disease, typically affecting early middle-aged males. Cutaneous and renal involvement were present in 45% of
cases and central nervous system involvement in 20%. Peripheral neuropathy occurred in 15% of cases [1]. In the more recent, larger series, clinical evidence of central nervous system involvement was detected in 20-30% of cases [7, 8]. Presenting features related to the nervous system include peripheral neuropathy, headache, blindness, cranial nerve palsies, hemiparesis, ataxia and altered consciousness [9]. CNS involvement has been stated by some authors to carry a poor prognosis [8, 10] though others have refuted this [11]. Peripheral neuropathy alone does not affect the outcome [8, 10]. The prognosis is generally poor with a median survival of 14 months [8]. Corticosteroids, cytotoxic chemotherapy, radiotherapy and surgery have all been reported to be of benefit though the paucity of cases available for a given trial has made assessment of results difficult [2, 8, 10]. Long term survival without treatment is also recognized [10, 13]. When pulmonary involvement is present, radiographic findings include bilateral lower zone-predominant pulmonary nodules, coalescent and cavitating pulmonary masses, diffuse or focal interstitial pulmonary infiltrates, plate atelectasis and pleural effusion. Hilar lymph node enlargement is unusual [1]. The nature of lymphomatoid granulomatosis, and in particular its relationship to lymphoma, has remained controversial ever since the first description, despite the advent of immunohistological and molecular biology techniques [1, 6, 10, 11]. Most authorities now consider LG to be part of the family of post-thymic T cell proliferations or peripheral T cell lymphomas [6, 14] though it is acknowledged that pathological heterogeneity exists [6]. Lymphomatoid granulomatosis may occur in the setting of a previous lymphoid primary tumour or immunosuppression and may itself progress to lymphoma in 12% of cases [8]. A recent report of LG coexisting with CNS lymphoma in patients with AIDS [15] has added to the controversy over the relationship between these two disorders [6]. Central nervous system involvement by LG may result pathologically in solid or necrotic masses, leptomeningeal and parenchymal infiltrates, infarction, haemorrhage and aneurysm formation [4, 5]. True infarctive necrosis probably occurs relatively rarely, though central tumour type necrosis is frequently observed [6]. There are relatively few descriptions of the CT and MR imaging appearances of CNS lesions of lymphomatoid granulomatosis and most are based on case reports or small series. The lesions are most frequently unifocal [2, 3, 5, 12] though multifocal lesions both above and below the tentorium have been described [4, 5]. Periventricular [3], temporal, temporoparietal [2, 4, 5] or posterior fossa [5, 12] lesions have been reported and some are haemorrhagic [5]. Oedema, mass effect, inhomogeneity, and variable contrast enhancement on CT have all been documented [2, 4, 5, 12]. In the absence of pulmonary or other systemic manifestations, the lesions have been mistaken for intrinsic tumours [2, 12] and demyelination [3]. The diagnosis has frequently only been made at autopsy [3-5]. Differentiation by MR imaging between inflammatory, infectious and neoplastic pathologies remains limited. Primary CNS lymphoma tends to be solitary, situated in the
27t deep parietal lobe and to be without significant mass effect; modest hyperintensity on T2-weighted SE images is c o m m o n [16]. Multiple sclerosis, concentric sclerosis, diffuse glioma or vasculitides may all cause diagnostic confusion [17]. High signal intensity periventricular lesions on T2-weighted images are a c o m m o n finding, and, in a recent paper, the possible causes discussed included MS, SLE, multifocal leukoencephalopathy, A I D S encephalitis, post-radiotherapy change, subependymal tumour, hydrocephalus, p s e u d o t u m o u r cerebri, vitamin B 12 deficiency, l y m p h o m a t o i d granulomatosis, Binswanger encephalopathy, multiple cerebral infarcts and neurosarcoidosis [18]. Infiltration of lepto-meningeal disease along the Virchow-Robin spaces and consequent parenchymal change occurs in both lymphomatoid granulomatosis [2, 5, 9] and neurosarcoidosis [18], and this m a y result in a similar pattern of lesions in both diseases. G a d o l i n i u m - D T P A enhanced M R imaging has recently been reported to confer greater sensitivity in the detection of lepto-meningeal neurosarcoidosis [19]. However, it remains highly unlikely that any imaging technique will permit a specific diagnosis to be m a d e and biopsy m a y still be required. The clinical presentation of CNS l y m p h o m a t o i d granulomatosis may be non-specific and the diagnosis elusive, especially when pulmonary disease is absent. CT and M R imaging of CNS lesions of L G may demonstrate a wide spectrum of appearances, reflecting the varied pathology. Biopsy m a y be essential if an accurate diagnosis is to be made and appropriate therapy instituted at an early stage.
Acknowledgements'. We thank Dr. G. S. Venables, Consultant Neurologist at the Royal Hallamshire Hospital, Sheffield for permission to report this case. Dr. R. W. Kerslake gratefully acknowledges support from the DH and MRC.
References i. Liebow AA, Carrington CRB, Friedman PJ (1972) Lymphomatoid granulomatosis. Hum Pathol 3:457-558 2. Kerr RSC, Hughes JT, Blamires T, Teddy PJ (1987) Lymphomatoid granulomatosis apparently confined to one temporal lobe. J Neurosurg 67:612-615 3. Smith A, Huang E, Weinstein MA (1990) Periventricular involvement in CNS lymphomatoid granulomatosis: MR demonstration. JCAT 14:291-293 4. Sackett JF, Zurhein GM, Bhimani SM (1979) Lymphomatoid granulomatosis involving the central nervous system: radiological-pathologic correlation. A JR 132:823-826
5. Kapila A, Gupta KL, Garcia JH (1988) CT and MR of lymphomatoid granulomatosis of the CNS: report of four cases and review of the literature. AJNR 9:1139-1143 6. Colby TV (1989) Central nervous system lymphomatoid granulomatosis in AIDS? Hum Patho120:301-302 7. Fauci AS, Haynes BF, Costa J, Katz R Wolff SM (1982) Lymphomatoid granulomatosis. Prospective clinical and therapeutic experience over 10 years. N Engl J Med 306:68-74 8. Katzenstein ALA, Carrington CRB, Liebow AA (1979) Lymphomatoid granulomatosis. A clinicopathological study of 152 cases. Cancer 43:360-473 9. Verity MA (1980) Cerebral lymphomatoid granulomatosis. In: Vinken PJ, Bruyn GW (eds) Handbook of clinical neurology vo139. (Neurological manifestations of systemic disease, part II) North-Holland Publishing, Amsterdam, pp 517-536 10. Pisani R J, DeRemee RA (1990) Clinical implications of the histopathological diagnosis of pulmonary lymphomatoid granulomatosis. Mayo Clin Proc 65:151-153 11. Koss MN, Hochholzer L, Langloss JM, Wehunt WD, Lazarus AA, Nichols PW (1986) Lymphomatoid granulomatosis: a clinicopathologic study of 42 patients. Pathology 18:283-288 12. Podlas HB, Gritzman MCD,Thomaides S, Roos H (1988) CTof CNS lesions in lymphomatoid granulomatosis: case report. AJNR 9:592-594 13. Firstater E, Yust I, Topilsky M, Tartakowsky B, Segal S, Abramov A (1983) Lymphomatoid granulomatosis with impaired cellular immunity Eight year survival without treatment. Chest 84:777-779 14. Myers JL (1990) Lymphomatoid granulomatosis: past, present, 9 future? Mayo Clin Proc 65:274-278 15. Anders KH, Latta H, Chang BS, Tomiyasu U, Quddusi AS, Vinters HV (1989) Lymphomatoid granulomatosis and malignant lymphoma of the central nervous system in the acquired immunodeficiency syndrome. Hum Patho120: 326-334 16. Schwiaghofer BW, Hesselink JR, Press GA, Wolf RL, Healy ME, Berthoty DP (1989) Primary intracranial CNS lymphoma: MR manifestations. AJNR 10:725-729 17. Valk J, Knaap vd MS (1989) Magnetic resonance imaging of myelin, myelination and myelination disorders. Springer, Berlin Heidelberg New York 18. Smith AS, Meisler DM, Weinstein MA, Tomsak RL, Hanson RL, Rudick RA, Farris BK, Ranoshoff RM (1989) High-signal periventricular lesions in patients with sarcoidosis: neurosarcoidosis or multiple sclerosis? AJNR 10:485-490 19. Sherman JL, Stern BA (1990) Gd-DTPA enhanced MRI of CNS sarcoidosis. XIV Symposium Neuroradiologicum, London, Book of abstracts P 125. Springer, Berlin Heidelberg New York
Dr. R. Kerslake Department of Radiology Queens Medical Centre Nottingham, NG7 2UH, UK
Neuro--
radiology 0 Springer-Verlag1991
CT and MR imaging of CNS lymphomatoid granulomatosis R. Kerslake 1 D. Rowe 2, and B. S. Worthington 1 Department of Radiology,Queen's MedicalCentre, Nottingham,UK 2 Department of Neurology,RoyalHallamshireHospital,Sheffield,UK Received: 24 July 1990
Summary. The clinical CT and MR imaging features of a pathologically confirmed case of lymphomatoid granulomatosis are presented. The disease was clinically confined to the central nervous system and the diagnosis was only made after brain biopsy had been performed. MR imaging revealed extensive non-confluent regions of white matter abnormality. Although uncommon, lymphomatoid granulomatosis should be included in the differential diagnosis of causes of periventricular and deep white matter lesions, even in the absence of pulmonary lesions. Specific therapy may produce clinical regression of disease. Key words: Brain, disease - Lymphomatoid granulomatosis - Brain, computed tomography- Brain, MR imaging Lymphomatoid granulomatosis (LG) is an "angiocentric and angiodestructive lymphorecticular proliferative and granulomatous disease" which predominantly involves the lungs [1]. A small number of cases with clinically isolated central nervous system (CNS) involvement at presentation have been reported [2, 3]. In the absence of systemic disease, the diagnosis may be considerably delayed or only made at autopsy [3-5]. We report a case of lymphomatoid granulomatosis clinically confined to the CNS in which the diagnosis was established by brain biopsy during the lifetime of the patient. Both CT and MR imaging demonstrated unusually extensive abnormalities though a specific diagnosis could not be made based on the imaging findings. Awareness of the spectrum of appearances on CT and MRI may permit the correct diagnosis to be suggested at an earlier stage, allowing institution of appropriate therapy.
Case report A 44-year-old female presented with a four week history of personality change, depression and irritability. She subsequently was observed to become increasingly weak, uncoordinated, obtunded and to develop an asymmetric
tetraparesis with a degree of ataxia. She was transferred from psychiatric to general medical and subsequently to neurological care. The only past history of note was a grade II-III CIN cervical lesion, treated by cone biopsy, with no evidence of recurrence at regular follow-up. At the time of admission to the neurological unit, she was afebrile, uncooperative and mute. There was no evidence of meningeal irritation or raised intracranial pressure. Neurological examination revealed an asymmetric spastic tetraparesis principally involving the left leg. An EEG showed widespread mixed irregular and rhythmic slow activity but without focal features. Cranial CT scanning (not shown) revealed multiple poorly defined regions of low attenuation in the basal ganglia, thalami and deep white matter of both cerebral hemispheres. These were without mass effect and showed no enhancement after the intravenous injection of iodinated contrast material. Examination of the CSF showed an elevated protein concentration (0.8 g/l) but no other abnormality. Chest radiography was entirely normal. MR imaging was carried out on a 0.15T resistive system. Multiple lesions were present in both cerebral hemispheres, the left cerebellar hemisphere and in the brain stem. The lesions were large, non-confluent, well demarcated and without mass effect. On T2-weighted images (Fig. i a) they were of high signal intensity whilst on inversion recovery images (Fig. 1 b), there was central hypointensity with a peripheral zone of intermediate signal intensity. Some of the larger lesions extended to involve the sub-cortical white matter. The corpus callosum was not involved. She deteriorated relentlessly and there was no response to a 5 day course of ACTH. Brain biopsy was then performed. The pathological findings were of white matter showing a heavy infiltrate of inflammatory cells which were principally large lymphocytes, plasma cells, histiocytes and some larger atypical cells with prominent nucleoli. The inflammatory infiltrate was markedly angiocentric and the walls of small vessels were infiltrated by a mixture of these chronic inflammatory cells. Patchy necrosis of the surrounding white matter was noted and
270
Fig. 1. Axial T2-weighted (SE 2000/80) images (a) and coronal inversion recovery (IR 1660/400/40)images (b) of biopsy-provenlymphomatoid granulomatosis. There are extensive, asymmetrical lesions mainly affecting the deep white matter of the right temporal lobe and external capsule, the left pons and cerebellar hemisphere and both posterior frontal/parietal lobes.Further lesions are present in the left parieto-occipital cortex these regions contained foamy histiocytes and some reactive histiocytes. A pathological diagnosis of lymphomatoid granulomatosis was made. Treatment with pulsed methylprednisolone and cyclophosphamide was commenced and the progressive improvement in her physical state was such that discharge to the community was possible 4 months after first presentation. She relapsed clinically 3 months later. There was clinical improvement following a further course of methylprednisolone and cyclophosphamide.
Discussion
In the original description of lymphomatoid granulomatosis in 1972, Liebow described a predominantly pulmonary disease, typically affecting early middle-aged males. Cutaneous and renal involvement were present in 45% of
cases and central nervous system involvement in 20%. Peripheral neuropathy occurred in 15% of cases [1]. In the more recent, larger series, clinical evidence of central nervous system involvement was detected in 20-30% of cases [7, 8]. Presenting features related to the nervous system include peripheral neuropathy, headache, blindness, cranial nerve palsies, hemiparesis, ataxia and altered consciousness [9]. CNS involvement has been stated by some authors to carry a poor prognosis [8, 10] though others have refuted this [11]. Peripheral neuropathy alone does not affect the outcome [8, 10]. The prognosis is generally poor with a median survival of 14 months [8]. Corticosteroids, cytotoxic chemotherapy, radiotherapy and surgery have all been reported to be of benefit though the paucity of cases available for a given trial has made assessment of results difficult [2, 8, 10]. Long term survival without treatment is also recognized [10, 13]. When pulmonary involvement is present, radiographic findings include bilateral lower zone-predominant pulmonary nodules, coalescent and cavitating pulmonary masses, diffuse or focal interstitial pulmonary infiltrates, plate atelectasis and pleural effusion. Hilar lymph node enlargement is unusual [1]. The nature of lymphomatoid granulomatosis, and in particular its relationship to lymphoma, has remained controversial ever since the first description, despite the advent of immunohistological and molecular biology techniques [1, 6, 10, 11]. Most authorities now consider LG to be part of the family of post-thymic T cell proliferations or peripheral T cell lymphomas [6, 14] though it is acknowledged that pathological heterogeneity exists [6]. Lymphomatoid granulomatosis may occur in the setting of a previous lymphoid primary tumour or immunosuppression and may itself progress to lymphoma in 12% of cases [8]. A recent report of LG coexisting with CNS lymphoma in patients with AIDS [15] has added to the controversy over the relationship between these two disorders [6]. Central nervous system involvement by LG may result pathologically in solid or necrotic masses, leptomeningeal and parenchymal infiltrates, infarction, haemorrhage and aneurysm formation [4, 5]. True infarctive necrosis probably occurs relatively rarely, though central tumour type necrosis is frequently observed [6]. There are relatively few descriptions of the CT and MR imaging appearances of CNS lesions of lymphomatoid granulomatosis and most are based on case reports or small series. The lesions are most frequently unifocal [2, 3, 5, 12] though multifocal lesions both above and below the tentorium have been described [4, 5]. Periventricular [3], temporal, temporoparietal [2, 4, 5] or posterior fossa [5, 12] lesions have been reported and some are haemorrhagic [5]. Oedema, mass effect, inhomogeneity, and variable contrast enhancement on CT have all been documented [2, 4, 5, 12]. In the absence of pulmonary or other systemic manifestations, the lesions have been mistaken for intrinsic tumours [2, 12] and demyelination [3]. The diagnosis has frequently only been made at autopsy [3-5]. Differentiation by MR imaging between inflammatory, infectious and neoplastic pathologies remains limited. Primary CNS lymphoma tends to be solitary, situated in the
27t deep parietal lobe and to be without significant mass effect; modest hyperintensity on T2-weighted SE images is c o m m o n [16]. Multiple sclerosis, concentric sclerosis, diffuse glioma or vasculitides may all cause diagnostic confusion [17]. High signal intensity periventricular lesions on T2-weighted images are a c o m m o n finding, and, in a recent paper, the possible causes discussed included MS, SLE, multifocal leukoencephalopathy, A I D S encephalitis, post-radiotherapy change, subependymal tumour, hydrocephalus, p s e u d o t u m o u r cerebri, vitamin B 12 deficiency, l y m p h o m a t o i d granulomatosis, Binswanger encephalopathy, multiple cerebral infarcts and neurosarcoidosis [18]. Infiltration of lepto-meningeal disease along the Virchow-Robin spaces and consequent parenchymal change occurs in both lymphomatoid granulomatosis [2, 5, 9] and neurosarcoidosis [18], and this m a y result in a similar pattern of lesions in both diseases. G a d o l i n i u m - D T P A enhanced M R imaging has recently been reported to confer greater sensitivity in the detection of lepto-meningeal neurosarcoidosis [19]. However, it remains highly unlikely that any imaging technique will permit a specific diagnosis to be m a d e and biopsy m a y still be required. The clinical presentation of CNS l y m p h o m a t o i d granulomatosis may be non-specific and the diagnosis elusive, especially when pulmonary disease is absent. CT and M R imaging of CNS lesions of L G may demonstrate a wide spectrum of appearances, reflecting the varied pathology. Biopsy m a y be essential if an accurate diagnosis is to be made and appropriate therapy instituted at an early stage.
Acknowledgements'. We thank Dr. G. S. Venables, Consultant Neurologist at the Royal Hallamshire Hospital, Sheffield for permission to report this case. Dr. R. W. Kerslake gratefully acknowledges support from the DH and MRC.
References i. Liebow AA, Carrington CRB, Friedman PJ (1972) Lymphomatoid granulomatosis. Hum Pathol 3:457-558 2. Kerr RSC, Hughes JT, Blamires T, Teddy PJ (1987) Lymphomatoid granulomatosis apparently confined to one temporal lobe. J Neurosurg 67:612-615 3. Smith A, Huang E, Weinstein MA (1990) Periventricular involvement in CNS lymphomatoid granulomatosis: MR demonstration. JCAT 14:291-293 4. Sackett JF, Zurhein GM, Bhimani SM (1979) Lymphomatoid granulomatosis involving the central nervous system: radiological-pathologic correlation. A JR 132:823-826
5. Kapila A, Gupta KL, Garcia JH (1988) CT and MR of lymphomatoid granulomatosis of the CNS: report of four cases and review of the literature. AJNR 9:1139-1143 6. Colby TV (1989) Central nervous system lymphomatoid granulomatosis in AIDS? Hum Patho120:301-302 7. Fauci AS, Haynes BF, Costa J, Katz R Wolff SM (1982) Lymphomatoid granulomatosis. Prospective clinical and therapeutic experience over 10 years. N Engl J Med 306:68-74 8. Katzenstein ALA, Carrington CRB, Liebow AA (1979) Lymphomatoid granulomatosis. A clinicopathological study of 152 cases. Cancer 43:360-473 9. Verity MA (1980) Cerebral lymphomatoid granulomatosis. In: Vinken PJ, Bruyn GW (eds) Handbook of clinical neurology vo139. (Neurological manifestations of systemic disease, part II) North-Holland Publishing, Amsterdam, pp 517-536 10. Pisani R J, DeRemee RA (1990) Clinical implications of the histopathological diagnosis of pulmonary lymphomatoid granulomatosis. Mayo Clin Proc 65:151-153 11. Koss MN, Hochholzer L, Langloss JM, Wehunt WD, Lazarus AA, Nichols PW (1986) Lymphomatoid granulomatosis: a clinicopathologic study of 42 patients. Pathology 18:283-288 12. Podlas HB, Gritzman MCD,Thomaides S, Roos H (1988) CTof CNS lesions in lymphomatoid granulomatosis: case report. AJNR 9:592-594 13. Firstater E, Yust I, Topilsky M, Tartakowsky B, Segal S, Abramov A (1983) Lymphomatoid granulomatosis with impaired cellular immunity Eight year survival without treatment. Chest 84:777-779 14. Myers JL (1990) Lymphomatoid granulomatosis: past, present, 9 future? Mayo Clin Proc 65:274-278 15. Anders KH, Latta H, Chang BS, Tomiyasu U, Quddusi AS, Vinters HV (1989) Lymphomatoid granulomatosis and malignant lymphoma of the central nervous system in the acquired immunodeficiency syndrome. Hum Patho120: 326-334 16. Schwiaghofer BW, Hesselink JR, Press GA, Wolf RL, Healy ME, Berthoty DP (1989) Primary intracranial CNS lymphoma: MR manifestations. AJNR 10:725-729 17. Valk J, Knaap vd MS (1989) Magnetic resonance imaging of myelin, myelination and myelination disorders. Springer, Berlin Heidelberg New York 18. Smith AS, Meisler DM, Weinstein MA, Tomsak RL, Hanson RL, Rudick RA, Farris BK, Ranoshoff RM (1989) High-signal periventricular lesions in patients with sarcoidosis: neurosarcoidosis or multiple sclerosis? AJNR 10:485-490 19. Sherman JL, Stern BA (1990) Gd-DTPA enhanced MRI of CNS sarcoidosis. XIV Symposium Neuroradiologicum, London, Book of abstracts P 125. Springer, Berlin Heidelberg New York
Dr. R. Kerslake Department of Radiology Queens Medical Centre Nottingham, NG7 2UH, UK
